Consistent with this hypothesis, inhibition of SOCE by overexpressing Orai2 results in the increased production of Aβ1–42 in SH-SY5Y and human neuroglioma H4 cells, suggesting a potential way to rescue the defects of AD and prevent the formation of APs by downregulating the expression of Orai2 [157,158]. The gene discussed is ORAI2; the disease is Alzheimer disease.